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152. Disruption of Ca2+i Homeostasis and Connexin 43 Hemichannel Function in the Right Ventricle Precedes Overt Arrhythmogenic Cardiomyopathy in Plakophilin-2-Deficient Mice.

Author

Kim, Joon-Chul, Pérez-Hernández, Marta, Alvarado, Francisco J., Maurya, Svetlana R., Montnach, Jerome, Yin, Yandong, Zhang, Mingliang, Lin, Xianming, Vasquez, Carolina, Heguy, Adriana, Liang, Feng-Xia, Woo, Sun-Hee, Morley, Gregory E., Rothenberg, Eli, Lundby, Alicia, Valdivia, Hector H., Cerrone, Marina, and Delmar, Mario

Published
2019
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153. Multilevel analyses of SCN5A mutations in arrhythmogenic right ventricular dysplasia/cardiomyopathy suggest non-canonical mechanisms for disease pathogenesis

Author

Te Riele, Anneline S J M, Agullo-Pascual, Esperanza, James, Cynthia A., Leo-Macias, Alejandra, Cerrone, Marina, Zhang, Mingliang, Lin, Xianming, Lin, Bin, Rothenberg, Eli, Sobreira, Nara L., Amat-Alarcon, Nuria, Marsman, Roos F., Murray, Brittney, Tichnell, Crystal, Van Der Heijden, Jeroen F., Dooijes, Dennis, Van Veen, Toon A B, Tandri, Harikrishna, Fowler, Steven J., Hauer, Richard N W, Tomaselli, Gordon, Van Den Berg, Maarten P., Taylor, Matthew R G, Brun, Francesca, Sinagra, Gianfranco, Wilde, Arthur A M, Mestroni, Luisa, Bezzina, Connie R., Calkins, Hugh, Van Tintelen, J. Peter, Bu, Lei, Delmar, Mario, Judge, Daniel P., Te Riele, Anneline S J M, Agullo-Pascual, Esperanza, James, Cynthia A., Leo-Macias, Alejandra, Cerrone, Marina, Zhang, Mingliang, Lin, Xianming, Lin, Bin, Rothenberg, Eli, Sobreira, Nara L., Amat-Alarcon, Nuria, Marsman, Roos F., Murray, Brittney, Tichnell, Crystal, Van Der Heijden, Jeroen F., Dooijes, Dennis, Van Veen, Toon A B, Tandri, Harikrishna, Fowler, Steven J., Hauer, Richard N W, Tomaselli, Gordon, Van Den Berg, Maarten P., Taylor, Matthew R G, Brun, Francesca, Sinagra, Gianfranco, Wilde, Arthur A M, Mestroni, Luisa, Bezzina, Connie R., Calkins, Hugh, Van Tintelen, J. Peter, Bu, Lei, Delmar, Mario, and Judge, Daniel P.

Published
2017

154. Regulation of cardiovascular connexins by mechanical forces and junctions

Author

Meens, Merlijn J., Pfenniger, Anna, Kwak, Brenda R., Delmar, Mario, Meens, Merlijn J., Pfenniger, Anna, Kwak, Brenda R., and Delmar, Mario

Abstract

Connexins form a family of transmembrane proteins that consists of 20 members in humans and 21 members in mice. Six connexins assemble into a connexon that can function as a hemichannel or connexon that can dock to a connexon expressed by a neighbouring cell, thereby forming a gap junction channel. Such intercellular channels synchronize responses in multicellular organisms through direct exchange of ions, small metabolites, and other second messenger molecules between the cytoplasms of adjacent cells. Multiple connexins are expressed in the cardiovascular system. These connexins not only experience the different biomechanical forces within this system, but may also act as effector proteins in co-ordinating responses within groups of cells towards these forces. This review discusses recent insights regarding regulation of cardiovascular connexins by mechanical forces and junctions. It specifically addresses effects of (i) shear stress on endothelial connexins, (ii) hypertension on vascular connexins, and (iii) changes in afterload and the composition of myocardial mechanical junctions on cardiac connexins

Published
2017

155. Plakophilin-2 is required for transcription of genes that control calcium cycling and cardiac rhythm

Author

Conductiegroep, Circulatory Health, Medische Fysiologie, Cerrone, Marina, Montnach, Jerome, Lin, Xianming, Zhao, Yan Ting, Zhang, Mingliang, Agullo-Pascual, Esperanza, Leo-Macias, Alejandra, Alvarado, Francisco J., Dolgalev, Igor, Karathanos, Thomas V., Malkani, Kabir, Van Opbergen, Chantal J.M., Van Bavel, Joanne J.A., Yang, Hua Qian, Vasquez, Carolina, Tester, David, Fowler, Steven J, Liang, Fengxia, Rothenberg, Eli, Heguy, Adriana, Morley, Gregory E., Coetzee, William A., Trayanova, Natalia A., Ackerman, Michael J., Van Veen, Toon A.B., Valdivia, Hector H., Delmar, Mario, Conductiegroep, Circulatory Health, Medische Fysiologie, Cerrone, Marina, Montnach, Jerome, Lin, Xianming, Zhao, Yan Ting, Zhang, Mingliang, Agullo-Pascual, Esperanza, Leo-Macias, Alejandra, Alvarado, Francisco J., Dolgalev, Igor, Karathanos, Thomas V., Malkani, Kabir, Van Opbergen, Chantal J.M., Van Bavel, Joanne J.A., Yang, Hua Qian, Vasquez, Carolina, Tester, David, Fowler, Steven J, Liang, Fengxia, Rothenberg, Eli, Heguy, Adriana, Morley, Gregory E., Coetzee, William A., Trayanova, Natalia A., Ackerman, Michael J., Van Veen, Toon A.B., Valdivia, Hector H., and Delmar, Mario

Published
2017

156. Multilevel analyses of SCN5A mutations in arrhythmogenic right ventricular dysplasia/cardiomyopathy suggest non-canonical mechanisms for disease pathogenesis

Author

Cardiologie Arts-onderzoekers, Team Onderzoek, Cardiologie, Circulatory Health, Team Medisch, Genetica Sectie Genoomdiagnostiek, Medische Fysiologie, Conductiegroep, Te Riele, Anneline S J M, Agullo-Pascual, Esperanza, James, Cynthia A., Leo-Macias, Alejandra, Cerrone, Marina, Zhang, Mingliang, Lin, Xianming, Lin, Bin, Rothenberg, Eli, Sobreira, Nara L., Amat-Alarcon, Nuria, Marsman, Roos F., Murray, Brittney, Tichnell, Crystal, Van Der Heijden, Jeroen F., Dooijes, Dennis, Van Veen, Toon A B, Tandri, Harikrishna, Fowler, Steven J., Hauer, Richard N W, Tomaselli, Gordon, Van Den Berg, Maarten P., Taylor, Matthew R G, Brun, Francesca, Sinagra, Gianfranco, Wilde, Arthur A M, Mestroni, Luisa, Bezzina, Connie R., Calkins, Hugh, Van Tintelen, J. Peter, Bu, Lei, Delmar, Mario, Judge, Daniel P., Cardiologie Arts-onderzoekers, Team Onderzoek, Cardiologie, Circulatory Health, Team Medisch, Genetica Sectie Genoomdiagnostiek, Medische Fysiologie, Conductiegroep, Te Riele, Anneline S J M, Agullo-Pascual, Esperanza, James, Cynthia A., Leo-Macias, Alejandra, Cerrone, Marina, Zhang, Mingliang, Lin, Xianming, Lin, Bin, Rothenberg, Eli, Sobreira, Nara L., Amat-Alarcon, Nuria, Marsman, Roos F., Murray, Brittney, Tichnell, Crystal, Van Der Heijden, Jeroen F., Dooijes, Dennis, Van Veen, Toon A B, Tandri, Harikrishna, Fowler, Steven J., Hauer, Richard N W, Tomaselli, Gordon, Van Den Berg, Maarten P., Taylor, Matthew R G, Brun, Francesca, Sinagra, Gianfranco, Wilde, Arthur A M, Mestroni, Luisa, Bezzina, Connie R., Calkins, Hugh, Van Tintelen, J. Peter, Bu, Lei, Delmar, Mario, and Judge, Daniel P.

Published
2017

158. Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias

Author

Bao, Yangyang, primary, Willis, B. Cicero, additional, Frasier, Chad R., additional, Lopez-Santiago, Luis F., additional, Lin, Xianming, additional, Ramos-Mondragón, Roberto, additional, Auerbach, David S., additional, Chen, Chunling, additional, Wang, Zhenxun, additional, Anumonwo, Justus, additional, Valdivia, Héctor H., additional, Delmar, Mario, additional, Jalife, José, additional, and Isom, Lori L., additional

Published
2016
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159. Transcription factor ETV1 is essential for rapid conduction in the heart

Author

Shekhar, Akshay, primary, Lin, Xianming, additional, Liu, Fang-Yu, additional, Zhang, Jie, additional, Mo, Huan, additional, Bastarache, Lisa, additional, Denny, Joshua C., additional, Cox, Nancy J., additional, Delmar, Mario, additional, Roden, Dan M., additional, Fishman, Glenn I., additional, and Park, David S., additional

Published
2016
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165. Disruption of Ca2+iHomeostasis and Connexin 43 Hemichannel Function in the Right Ventricle Precedes Overt Arrhythmogenic Cardiomyopathy in Plakophilin-2–Deficient Mice

Author

Kim, Joon-Chul, Pérez-Hernández, Marta, Alvarado, Francisco J., Maurya, Svetlana R., Montnach, Jerome, Yin, Yandong, Zhang, Mingliang, Lin, Xianming, Vasquez, Carolina, Heguy, Adriana, Liang, Feng-Xia, Woo, Sun-Hee, Morley, Gregory E., Rothenberg, Eli, Lundby, Alicia, Valdivia, Hector H., Cerrone, Marina, and Delmar, Mario

Abstract

Supplemental Digital Content is available in the text.

Published
2019
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167. Gap junctions-guards of excitability

Author

Stroemlund, Line Waring, Jensen, Christa Funch, Qvortrup, Klaus, Delmar, Mario, Nielsen, Morten Schak, Stroemlund, Line Waring, Jensen, Christa Funch, Qvortrup, Klaus, Delmar, Mario, and Nielsen, Morten Schak

Abstract

Cardiomyocytes are connected by mechanical and electrical junctions located at the intercalated discs (IDs). Although these structures have long been known, it is becoming increasingly clear that their components interact. This review describes the involvement of the ID in electrical disturbances of the heart and focuses on the role of the gap junctional protein connexin 43 (Cx43). Current evidence shows that Cx43 plays a crucial role in organizing microtubules at the intercalated disc and thereby regulating the trafficking of the cardiac sodium channel NaV1.5 to the membrane.

Published
2015

171. Gap junction protein Cx37 interacts with endothelial nitric oxide synthase in endothelial cells

Author

Pfenniger Anna, Derouette Jean-Paul, Verma Vandana, Lin Xianming, Foglia Bernard, Coombs Wanda, Roth Isabelle, Satta Nathalie, Dunoyer-Geindre Sylvie, Sorgen Paul, Taffet Steven, Kwak Brenda R, Delmar Mario, Miquerol L, Deutsch U, Jongsma H J, Chanson M, and Kwak B R

Subjects
Patch-Clamp Techniques, Amino Acid Motifs, Plasma protein binding, 030204 cardiovascular system & hematology, Connexins, Membrane Potentials, chemistry.chemical_compound, Mice, 0302 clinical medicine, Enos, Connexins/genetics/*metabolism, Cross-Linking Reagents/chemistry, Cells, Cultured, ddc:616, 0303 health sciences, Nitric Oxide Synthase Type III, Transfection, Nitric oxide synthase, Endothelial stem cell, Cross-Linking Reagents, Biochemistry, Recombinant Fusion Proteins/metabolism, Cardiology and Cardiovascular Medicine, Protein Binding, Endothelial Cells/*enzymology, Recombinant Fusion Proteins, Nitric Oxide Synthase Type III/genetics/*metabolism, Biology, Nitric Oxide, Article, Nitric oxide, 03 medical and health sciences, Peptide Library, Animals, Humans, Immunoprecipitation, Binding site, 030304 developmental biology, Binding Sites, Polymorphism, Genetic, Endothelial Cells, Surface Plasmon Resonance, biology.organism_classification, Molecular biology, chemistry, Connexin 43, Nitric Oxide/metabolism, biology.protein, Connexin 43/metabolism
Abstract

Objective— The gap junction protein connexin37 (Cx37) plays an important role in cell-cell communication in the vasculature. A C1019T Cx37 gene polymorphism, encoding a P319S substitution in the regulatory C terminus of Cx37 (Cx37CT), correlates with arterial stenosis and myocardial infarction in humans. This study was designed to identify potential binding partners for Cx37CT and to determine whether the polymorphism modified this interaction. Methods and Results— Using a high-throughput phage display, we retrieved 2 binding motifs for Cx37CT: WHK … [K,R]XP … and FHK … [K,R]XXP … , the first being more common for Cx37CT-319P and the second more common for Cx37CT-319S. One of the peptides (WHRTPRLPPPVP) showed 77.7% homology with residues 843 to 854 of endothelial nitric oxide synthase (eNOS). In vitro binding of this peptide or of the homologous eNOS sequence to both Cx37CT isoforms was confirmed by cross-linking and surface plasmon resonance. Electrophysiological analysis of Cx37 single channel activity in transfected N2a cells showed that eNOS-like and eNOS(843–854) increased the frequency of events with conductances higher than 300 pS. We demonstrated that eNOS coimmunoprecipitated with Cx37 in a mouse endothelial cell (EC) line (bEnd.3), human primary ECs, and a human EC line transfected with Cx37-319P or Cx37-319S. Cx37 and eNOS colocalized at EC membranes. Moreover, a dose-dependent increase in nitric oxide production was observed in ECs treated with Cx37 antisense. Conclusion— Overall, our data show for the first time a functional and specific interaction between eNOS and Cx37. This interaction may be relevant for the control of vascular physiology both in health and in disease.

Published
2010

176. Scn1b deletion leads to increased tetrodotoxin‐sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts

Author

Lin, Xianming, primary, O'Malley, Heather, additional, Chen, Chunling, additional, Auerbach, David, additional, Foster, Monique, additional, Shekhar, Akshay, additional, Zhang, Mingliang, additional, Coetzee, William, additional, Jalife, José, additional, Fishman, Glenn I., additional, Isom, Lori, additional, and Delmar, Mario, additional

Published
2014
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177. Missense Mutations in Plakophilin-2 Cause Sodium Current Deficit and Associate With a Brugada Syndrome Phenotype

Author

Cerrone, Marina, primary, Lin, Xianming, additional, Zhang, Mingliang, additional, Agullo-Pascual, Esperanza, additional, Pfenniger, Anna, additional, Chkourko Gusky, Halina, additional, Novelli, Valeria, additional, Kim, Changsung, additional, Tirasawadichai, Tiara, additional, Judge, Daniel P., additional, Rothenberg, Eli, additional, Chen, Huei-Sheng Vincent, additional, Napolitano, Carlo, additional, Priori, Silvia G., additional, and Delmar, Mario, additional

Published
2014
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178. A Connexin40 Mutation Associated With a Malignant Variant of Progressive Familial Heart Block Type I

Author

Makita, Naomasa, Seki, Akiko, Sumitomo, Naokata, Chkourko, Halina, Fukuhara, Shigetomo, Watanabe, Hiroshi, Shimizu, Wataru, Bezzina, Connie R., Hasdemir, Can, Mugishima, Hideo, Makiyama, Takeru, Baruteau, Alban, Baron, Estelle, Horie, Minoru, Hagiwara, Nobuhisa, Wilde, Arthur A.M., Probst, Vincent, Le, Marec Hervé, Roden, Dan M., Mochizuki, Naoki, Schott, Jean-Jacques, Delmar, Mario, Makita, Naomasa, Seki, Akiko, Sumitomo, Naokata, Chkourko, Halina, Fukuhara, Shigetomo, Watanabe, Hiroshi, Shimizu, Wataru, Bezzina, Connie R., Hasdemir, Can, Mugishima, Hideo, Makiyama, Takeru, Baruteau, Alban, Baron, Estelle, Horie, Minoru, Hagiwara, Nobuhisa, Wilde, Arthur A.M., Probst, Vincent, Le, Marec Hervé, Roden, Dan M., Mochizuki, Naoki, Schott, Jean-Jacques, and Delmar, Mario

Abstract

Background-Progressive familial heart block type I (PFHBI) is a hereditary arrhythmia characterized by progressive conduction disturbances in the His-Purkinje system. PFHBI has been linked to genes such as SCN5A that influence cardiac excitability but not to genes that influence cell-to-cell communication. Our goal was to explore whether nucleotide substitutions in genes coding for connexin proteins would associate with clinical cases of PFHBI and if so, to establish a genotype-cell phenotype correlation for that mutation. Methods and Results-We screened 156 probands with PFHBI. In addition to 12 sodium channel mutations, we found a germ line GJA5 (connexin40 [Cx40]) mutation (Q58L) in 1 family. Heterologous expression of Cx40-Q58L in connexin-deficient neuroblastoma cells resulted in marked reduction of junctional conductance (Cx40-wild type [WT], 22.2 ± 1.7 nS, n=14; Cx40-Q58L, 0.56 ± 0.34 nS, n=14; P <0.001) and diffuse localization of immunoreactive proteins in the vicinity of the plasma membrane without formation of gap junctions. Heteromeric cotransfection of Cx40-WT and Cx40-Q58L resulted in homogenous distribution of proteins in the plasma membrane rather than in membrane plaques in ̃ 50% of cells; well-defined gap junctions were observed in other cells. Junctional conductance values correlated with the distribution of gap junction plaques. Conclusions-Mutation Cx40-Q58L impairs gap junction formation at cell-cell interfaces. This is the first demonstration of a germ line mutation in a connexin gene that associates with inherited ventricular arrhythmias and emphasizes the importance of Cx40 in normal propagation in the specialized conduction system., Circulation: Arrhythmia and Electrophysiology, 5(1), pp.163-172; 2012

Published
2012

180. Phosphorylation of connexin43 on serine 306 regulates electrical coupling

Author

Procida, Kristina, Jørgensen, Lone, Schmitt, Nicole, Delmar, Mario, Taffet, Steven M, Holstein-Rathlou, Niels-Henrik, Nielsen, Morten Schak, Braunstein, Thomas Hartig, Procida, Kristina, Jørgensen, Lone, Schmitt, Nicole, Delmar, Mario, Taffet, Steven M, Holstein-Rathlou, Niels-Henrik, Nielsen, Morten Schak, and Braunstein, Thomas Hartig

Abstract

Udgivelsesdato: 2009-Nov, BACKGROUND: Phosphorylation is a key regulatory event in controlling the function of the cardiac gap junction protein connexin43 (Cx43). Three new phosphorylation sites (S296, S297, S306) have been identified on Cx43; two of these sites (S297 and S306) are dephosphorylated during ischemia. The functional significance of these new sites is currently unknown. OBJECTIVE: The purpose of this study was to examine the role of S296, S297, and S306 in the regulation of electrical intercellular communication. METHODS: To mimic constitutive dephosphorylation, serine was mutated to alanine at the three sites and expressed in HeLa cells. Electrical coupling and single channel measurements were performed by double patch clamp. Protein expression levels were assayed by western blotting, localization of Cx43, and phosphorylation of S306 by immunolabeling. Free hemichannels were assessed by biotinylation. RESULTS: Macroscopic conductance in cells expressing S306A was reduced to 57% compared to wild type (WT), whereas coupling was not significantly changed in cells expressing either S296A or S297A. S306A-expressing cells displayed similar protein and free hemichannel abundance compared to WT Cx43, whereas the fractional area of plaques in cell-to-cell interfaces was increased. However, single channel measurements showed a WT Cx43 main state conductance of 119 pS, whereas the main state conductance of S306A channels was reduced to 95 pS. Furthermore, channel gating was affected in S306A channels. CONCLUSION: Lack of phosphorylation at serine 306 results in reduced coupling, which can be explained by reduced single channel conductance. We suggest that dephosphorylation of S306 partly explains the electrical uncoupling seen in myocardial ischemia.

Published
2009

181. CE-452779-3 RANDOMIZED PLACEBO-CONTROLLED TRIAL OF FLECAINIDE IN PATIENTS WITH ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY.

Author

Zareba, Wojciech, Tichnell, Crystal, Rosero, Spencer Z., Cerrone, Marina, Zipse, Matthew M., Marchlinski, Francis E., Sun, Albert Y., Indik, Julia H., James, Cynthia A., Mestroni, Luisa, Cutter, Kristina, Peterson, Derick R., McNitt, Scott, Polonsky, Bronislava, Daubert, James P., Haigney, Mark C., Needleman, Matthew, Oakes, David, Delmar, Mario, and Calkins, Hugh

Published
2023
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184. RXP-E: a connexin43-binding peptide that prevents action potential propagation block

Author

Lewandowski, Rebecca, Procida, Kristina, Vaidyanathan, Ravi, Coombs, Wanda, Jalife, José, Nielsen, Morten S, Taffet, Steven M, Delmar, Mario, Lewandowski, Rebecca, Procida, Kristina, Vaidyanathan, Ravi, Coombs, Wanda, Jalife, José, Nielsen, Morten S, Taffet, Steven M, and Delmar, Mario

Abstract

Udgivelsesdato: 2008-Aug-29, Gap junctions provide a low-resistance pathway for cardiac electric propagation. The role of GJ regulation in arrhythmia is unclear, partly because of limited availability of pharmacological tools. Recently, we showed that a peptide called "RXP-E" binds to the carboxyl terminal of connexin43 and prevents chemically induced uncoupling in connexin43-expressing N2a cells. Here, pull-down experiments show RXP-E binding to adult cardiac connexin43. Patch-clamp studies revealed that RXP-E prevented heptanol-induced and acidification-induced uncoupling in pairs of neonatal rat ventricular myocytes. Separately, RXP-E was concatenated to a cytoplasmic transduction peptide (CTP) for cytoplasmic translocation (CTP-RXP-E). The effect of RXP-E on action potential propagation was assessed by high-resolution optical mapping in monolayers of neonatal rat ventricular myocytes, containing approximately 20% of randomly distributed myofibroblasts. In contrast to control experiments, when heptanol (2 mmol/L) was added to the superfusate of monolayers loaded with CTP-RXP-E, action potential propagation was maintained, albeit at a slower velocity. Similarly, intracellular acidification (pH(i) 6.2) caused a loss of action potential propagation in control monolayers; however, propagation was maintained in CTP-RXP-E-treated cells, although at a slower rate. Patch-clamp experiments revealed that RXP-E did not prevent heptanol-induced block of sodium currents, nor did it alter voltage dependence or amplitude of Kir2.1/Kir2.3 currents. RXP-E is the first synthetic molecule known to: (1) bind cardiac connexin43; (2) prevent heptanol and acidification-induced uncoupling of cardiac gap junctions; and (3) preserve action potential propagation among cardiac myocytes. RXP-E can be used to characterize the role of gap junctions in the function of multicellular systems, including the heart.

Published
2008

186. Deletion of the last five C-terminal amino acid residues of connexin43 leads to lethal ventricular arrhythmias in mice without affecting coupling via gap junction channels

Author

Lübkemeier, Indra, primary, Requardt, Robert Pascal, additional, Lin, Xianming, additional, Sasse, Philipp, additional, Andrié, René, additional, Schrickel, Jan Wilko, additional, Chkourko, Halina, additional, Bukauskas, Feliksas F., additional, Kim, Jung-Sun, additional, Frank, Marina, additional, Malan, Daniela, additional, Zhang, Jiong, additional, Wirth, Angela, additional, Dobrowolski, Radoslaw, additional, Mohler, Peter J., additional, Offermanns, Stefan, additional, Fleischmann, Bernd K., additional, Delmar, Mario, additional, and Willecke, Klaus, additional

Published
2013
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187. Remodeling of the cardiac sodium channel, connexin43, and plakoglobin at the intercalated disk in patients with arrhythmogenic cardiomyopathy

Author

Noorman, Maartje, primary, Hakim, Sara, additional, Kessler, Elise, additional, Groeneweg, Judith A, additional, Cox, Moniek G.P.J., additional, Asimaki, Angeliki, additional, van Rijen, Harold V.M., additional, van Stuijvenberg, Leonie, additional, Chkourko, Halina, additional, van der Heyden, Marcel A.G., additional, Vos, Marc A., additional, de Jonge, Nicolaas, additional, van der Smagt, Jasper J., additional, Dooijes, Dennis, additional, Vink, Aryan, additional, de Weger, Roel A., additional, Varro, Andras, additional, de Bakker, Jacques M.T., additional, Saffitz, Jeffrey E., additional, Hund, Thomas J., additional, Mohler, Peter J., additional, Delmar, Mario, additional, Hauer, Richard N.W., additional, and van Veen, Toon A.B., additional

Published
2013
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190. Heterogeneity of ATP-sensitive K+ Channels in Cardiac Myocytes

Author

Hong, Miyoun, primary, Bao, Li, additional, Kefaloyianni, Eirini, additional, Agullo-Pascual, Esperanza, additional, Chkourko, Halina, additional, Foster, Monique, additional, Taskin, Eylem, additional, Zhandre, Marine, additional, Reid, Dylan A., additional, Rothenberg, Eli, additional, Delmar, Mario, additional, and Coetzee, William A., additional

Published
2012
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192. Gap Junctions

Author

Nielsen, Morten Schak, primary, Nygaard Axelsen, Lene, additional, Sorgen, Paul L., additional, Verma, Vandana, additional, Delmar, Mario, additional, and Holstein‐Rathlou, Niels‐Henrik, additional

Published
2012
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195. Reduced heterogeneous expression of Cx43 results in decreased Nav1.5 expression and reduced sodium current that accounts for arrhythmia vulnerability in conditional Cx43 knockout mice

Author

Jansen, John A., primary, Noorman, Maartje, additional, Musa, Hassan, additional, Stein, Mèra, additional, de Jong, Sanne, additional, van der Nagel, Roel, additional, Hund, Thomas J., additional, Mohler, Peter J., additional, Vos, Marc A., additional, van Veen, Toon A., additional, de Bakker, Jacques M., additional, Delmar, Mario, additional, and van Rijen, Harold V., additional

Published
2012
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197. A Connexin40 Mutation Associated With a Malignant Variant of Progressive Familial Heart Block Type I

Author

Makita, Naomasa, primary, Seki, Akiko, additional, Sumitomo, Naokata, additional, Chkourko, Halina, additional, Fukuhara, Shigetomo, additional, Watanabe, Hiroshi, additional, Shimizu, Wataru, additional, Bezzina, Connie R., additional, Hasdemir, Can, additional, Mugishima, Hideo, additional, Makiyama, Takeru, additional, Baruteau, Alban, additional, Baron, Estelle, additional, Horie, Minoru, additional, Hagiwara, Nobuhisa, additional, Wilde, Arthur A.M., additional, Probst, Vincent, additional, Le Marec, Hervé, additional, Roden, Dan M., additional, Mochizuki, Naoki, additional, Schott, Jean-Jacques, additional, and Delmar, Mario, additional

Published
2012
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